Aim

The purpose of this study is to quantifiably determine if the Extended Longevity Protocol has a significant clinical effect on epigenetic age. Through the epigenetic age test we hope to see an impact on the epigenetic age within one year.

 

Rationale

Despite considerable effort, successful treatment of reversing one’s biological age has deemed to be a difficult therapeutic challenge. There is evidence that the Extended Longevity Protocol is a safe and effective treatment option to improve clinical care of healthy individual’s biological age.

 

Studies have shown that the Extended Longevity Protocol decelerates the Epigenome biomarkers of aging.

 

The participants in the Fahy study were given a combination of growth hormone and two types of diabetes medications during the study; on average, their biological ages were reduced by an average of 2.5 years, as measured by the epigenetic clock. This clock works by examining the epigenome, the alterations to gene expression that predictably change throughout lifespan and so can be reliably used to estimate a person’s biological age.

 

This measurement is a much more accurate way to determine the biological rather than chronological age of a person. Some people are epigenetically older or younger than they are chronologically, meaning that they have aged faster or slower, respectively. Such a measurement system is therefore ideal for measuring changes to biological age in order to test interventions that target the aging processes.

 

Background

Between 2015 and 2030, the number of people in the world aged 60 years or over is expected to grow by 56%, from just over 900 million to nearly 1.5 billion. By 2050, the global population of people older than 60 is expected to jump to two billion. In the United States, the number of Americans over the age of 65 is expected to double from roughly 50 million today to nearly 100 million by 2060. Population aging is going to have an increasing impact on healthcare in developed countries due to the increase in elder and long-term care.

 

Over the past three decades, there has been an increasing focus on decelerating and improving aging. Investigation in animal models has shown reversal in some aspects of aging and some ongoing studies are being carried out to slow the progression. But ultimately, aging is the result of a gradual functional decline at the cellular level. On a cellular level, aging is the result of somatic mammalian cells' natural tendency for cell division, after which they enter cellular senescence due to the irreversible growth. Cellular senescence entails irreversible cell cycle arrest. Senescent cells are characterized by their inability to proliferate, resistance to apoptosis, and secretion of factors that promote inflammation and tissue deterioration.

Resulting in the development of myriad chronic illness including heart disease, stroke and diabetes.

 

Chronic, sterile, low-grade inflammation — called inflammaging — develops, as a result of the accumulation of senescent cells. This inflammation creates a positive feedback loop which contributes to adverse age-related pathologies. In addition, the immune system can be affected as senescence increases by having fewer naive T Cells and more senescent T Cells leading to immunosenescence and dysfunction as we age.

 

Biological age compared to chronological age has become detrimental in determining one’s healthy aging process. Thus, the importance of predicting the state of one's biophysiological aging. One such biologic age predictor, measures DNA methylation levels, otherwise known as the epigenetic clock. The Fahy study showed that the epigenetic clock can officially predict one’s biological age with more accuracy than chronological age and has shown that epigenetic age in humans can be reversed.

 

Our research has determined that aging is largely controlled by ten (10) primary internal biological factors, now understood to be reversible. Here they are listed hierarchically, most important to least important:

 

1. Pineal clock- (Pineal / Hypothalmic/ Pituitary/ Superchiasmatic Nucleolus (SCN) axis) this is the master time clock and coordinates the body's circadian rhythm and the time-cycled release of melatonin and other critical hormones and neurotransmitters.

2. Thymic involution- immune depletion, and T-cell diminution.

3. Blood signaling and transcription factors- reverse distributed blood signaling of TGF-ß1 and Oxytocin (to all cells).

4. Telomere length- Attrition of the protective chromosomal endcaps causing programmed Cellular senescence.

5. Senolytics- (autophagy, mitophagy) Accumulation of senescent zombie-like cells that inflame and signal senescence to healthy cells.

6. Inflammaging- Inflammatory response, altered intercellular communication and the production of inflammatory cytokine and chemokine molecules.

7. Stem Cell Exhaustion- loss of source stem cells.

8. Cellular Metabolic Efficiency (NAD, NMN, NR, Sirtuins, Resveratrol, ATP, ROS)- Energy production and mitochondrial dysfunction.

9. Epigenetic clock (DNAm cytosine methylation)- Alterations to the epigenome that control which genes are turned on and off.

10. Extra Cellular Matrix Stiffening - The decrease in elastin, in turn, increases collagen content and ECM stiffness. This causes age-related diseases such as hypertension, and atherosclerosis.

 

• Two factors are endocrinological: Pineal/ Hypothalamic /Pituitary/ SCN axis, and Thymus involution, which are internal aging-clock related.

• Two factors are DNA based: Telomere length and Epigenetic DNA methylation, which are internal aging-clock related.

• Two factors are cellular: Cellular Metabolic Efficiency and Senolytics, and are adapted systemic responses.

• Four factors are Systemic: Blood signaling, Extra Cellular Matrix Stiffening, and Stem Cell Exhaustion, which are internal aging-clock related and Inflammaging, which is an adapted systemic response.

 

Current Standard of Care

Currently, there are no other alternative medications.